YAP/TAZ at the Roots of Cancer
Open accessAbstract
YAP and TAZ are highly related transcriptional regulators pervasively activated in human malignancies. Recent work indicates that, remarkably, YAP/TAZ are essential for cancer initiation or growth of most solid tumors. Their activation induces cancer stem cell attributes, proliferation, chemoresistance, and metastasis. YAP/TAZ are sensors of the structural and mechanical features of the cell microenvironment. A number of cancer-associated extrinsic and intrinsic cues conspire to overrule the YAP-inhibiting microenvironment of normal tissues, including changes in mechanotransduction, inflammation, oncogenic signaling, and regulation of the Hippo pathway. Addiction to YAP/TAZ thus potentially represents a central cancer vulnerability that may be exploited therapeutically.
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The Hippo pathway controls the YAP-TAZ-TEAD transcriptional complex that promotes expression of genes important for cancer cell proliferation, survival, and progression.
“The Hippo pathway controls the YAP-TAZ-TEAD transcriptional complex that promotes the expression of genes important for cancer cell proliferation, survival, and progression (26–28).”
From Targeting eIF4A-dependent translation in genetically complex sarcoma (2026) · cites this paper as [26]
YAP1 is dispensable for homeostasis of normal cells in adults.
“genetic studies in various mouse models suggest that YAP1 is dispensable for the homeostasis of normal cells in adults.45”
From Therapeutic targeting of syndecan-1 axis overcomes acquired resistance to KRAS-targeted therapy in gastrointestinal cancers (2025) · cites this paper as [45]
A capacity for small-molecule-mediated direct targeting of YAP remains elusive.
“While our data do support that YAP inhibitors may also exert synergistic effects to KRAS G12C inhibition, a capacity for small‐molecule‐mediated direct targeting of YAP remains elusive.[ 27 ]”
From Focal Adhesion Kinase (FAK) Inhibition Synergizes with KRAS G12C Inhibitors in Treating Cancer through the Regulation of the FAK–YAP Signaling (2021) · cites this paper as [27]
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“The AMPK kinase provides another mechanism by which glycolysis, and more generally energy metabolism, may feedback on YAP/TAZ: in this model, AMPK is induced by low energy conditions and attenuates YAP/TAZ function (DeRan et al., 2014; Mo et al., 2015; Wang et al., 2015b).”
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Canonical Wnt signalling activates TAZ through PP1A during osteogenic differentiation
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Deregulation of the Hippo pathway in soft-tissue sarcoma promotes FOXM1 expression and tumorigenesis
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A miR-130a-YAP positive feedback loop promotes organ size and tumorigenesis
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Prognostic Significance of TAZ Expression in Resected Non-Small Cell Lung Cancer
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YAP induces high-grade serous carcinoma in fallopian tube secretory epithelial cells
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Mutual interaction between YAP and c-Myc is critical for carcinogenesis in liver cancer
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Kaposi sarcoma-associated herpesvirus promotes tumorigenesis by modulating the Hippo pathway
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Clinical and prognostic significance of Yes-associated protein in colorectal cancer
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Functional and Clinical Evidence That TAZ is a Candidate Oncogene in Hepatocellular Carcinoma
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Yes-Associated Protein 1 Is Activated and Functions as an Oncogene in Meningiomas
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Alterations in the NF2/LATS1/LATS2/YAP Pathway in Schwannomas
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TAZ promotes temozolomide resistance by upregulating MCL-1 in human glioma cells
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Force triggers YAP nuclear entry by regulating transport across nuclear pores
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YAP/TAZ upstream signals and downstream responses
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Self-citationTargeting the Hippo pathway in cancer, fibrosis, wound healing and regenerative medicine
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The extracellular matrix in tumor progression and metastasis
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Comprehensive Molecular Characterization of the Hippo Signaling Pathway in Cancer
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Hepatocyte TAZ/WWTR1 Promotes Inflammation and Fibrosis in Nonalcoholic Steatohepatitis
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YAP-mediated mechanotransduction tunes the macrophage inflammatory response
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“Manipulation of YAP/TAZ is currently being explored as a therapeutic approach for a wide range of pathologies that involve macrophages and exhibit prominent changes in the biophysical tissue environment (23, 26, 27).”
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Extracellular matrix stiffness: Mechanisms in tumor progression and therapeutic potential in cancer
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“YAP is required for CAFs to promote matrix sclerosis, acting as a marker of CAFs at early tumor stages and as an inducer of mechanical activation of CAF function [5].”
InfluentialYAP-Induced PD-L1 Expression Drives Immune Evasion in BRAFi-Resistant Melanoma
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Interferon-γ induces tumor resistance to anti-PD-1 immunotherapy by promoting YAP phase separation
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Insights into recent findings and clinical application of YAP and TAZ in cancer
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SRC tyrosine kinase activates the YAP/TAZ axis and thereby drives tumor growth and metastasis
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Therapeutic targeting of TEAD transcription factors in cancer
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STAT3-YAP/TAZ signaling in endothelial cells promotes tumor angiogenesis
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TEAD Inhibition Overcomes YAP1/TAZ-Driven Primary and Acquired Resistance to KRASG12C Inhibitors
Edwards, A. C., Stalnecker, C. A., Jean Morales, A., Taylor, K. E., Klomp, J. E., Klomp, J. A., Waters, A. M., Sudhakar, N., Hallin, J., Tang, T. T., et al. (2023) · Cancer Research · doi:10.1158/0008-5472.can-23-2994 · Cited by 91 · see citing works
Endothelial YAP/TAZ Signaling in Angiogenesis and Tumor Vasculature
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Covalent disruptor of YAP-TEAD association suppresses defective Hippo signaling
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Targeting eIF4A-dependent translation in genetically complex sarcoma
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- Authors
- Zanconato, F., Cordenonsi, M., & Piccolo, S.
- Affiliations
- University of Padua (IT)
- Corresponding author
- Cordenonsi, Michelangelo
- Piccolo, Stefano
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2016-06
- Volume
- 29
- Issue
- 6
- Pages
- 783-803
- ISSN
- 1535-6108 (ISSN-L)
- PMC
- PMC6186419
- OpenAlex
- W2426003472
- Cited by
- 1,970
- References
- 221
- Citations by year
- 2026: 176 · 2025: 182 · 2024: 213 · 2023: 233 · 2022: 254 · 2021: 236 · 2020: 230 · 2019: 179 · 2018: 165 · 2017: 82 · 2016: 17
- FWCI
- 15.97
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cancer Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Padua Research Archive (University of Padova) (submittedVersion, other-oa)
- Funders
- Ministero dell’Istruzione, dell’Università e della Ricerca
- Associazione Italiana per la Ricerca sul Cancro
- European Research Council
- Horizon 2020 (670126-DENOVOSTEM)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hippo pathway signaling and YAP/TAZ
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Microtubule and mitosis dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer-related molecular mechanisms research
- Keywords
- YAP, TAZ, Hippo signaling pathway, tumor initiation, solid tumors, cancer stem cells, chemoresistance, metastasis, tumor microenvironment, mechanotransduction, inflammation, oncogenic signaling, cancer vulnerability, therapeutic target
- MeSH terms
- Hippo Signaling Pathway, YAP-Signaling Proteins, Transcriptional Coactivator with PDZ-Binding Motif Proteins, Animals, Humans, Neoplasms, Phosphoproteins, Transcription Factors, Neoplastic Stem Cells, Signal Transduction, Trans-Activators, Protein Serine-Threonine Kinases, Drug Resistance, Neoplasm, Mechanotransduction, Cellular, Intracellular Signaling Peptides and Proteins, Adaptor Proteins, Signal Transducing, Cell Proliferation, Tumor Microenvironment
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